Abstract
Leptin was originally identified as a peripheral satiety signal made by fat cells and it was proposed that as fat accumulates leptin is secreted proportionally. Leptin then crosses the blood brain barrier and signals to the hypothalamus suppressing appetite and increasing energy expenditure as it rises. It is evident that if the leptin gene or its receptor is disrupted them morbid obesity occurs. However, obesity in humans is very rarely caused by a disruption of the leptin gene or its receptor, and in many species a good correlation exists between leptin concentrations in plasma with the degree of obesity. This early finding was unexpected and led to the leptin resistance hypothesis. Further studies have revealed that leptin actually appears to be almost ubiquitously expressed in many tissues. Unfortunately despite the accumulation of a vast literature leptin still appears to be regarded as a peripheral satiety signal although the data to support this hypothesis is not substantial.
| Original language | English |
|---|---|
| Pages | 100-102 |
| Publication status | Published - 2008 |
| Event | ACVSc 2008 Conference: Australian College of Veterinary Scientists 2008 Annual Conference - Surfers Paradise, Australia Duration: 3 Jul 2008 → 5 Jul 2008 |
Conference
| Conference | ACVSc 2008 Conference: Australian College of Veterinary Scientists 2008 Annual Conference |
|---|---|
| City | Surfers Paradise, Australia |
| Period | 3/07/08 → 5/07/08 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Physiology
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